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Physio Exam 3 > L21/22 Cardiac Performance > Flashcards

L21/22 Cardiac Performance Flashcards

1
Q

Cardiac performance

A

Primary function = eject sufficing amount of blood into arterial system to maintain blood pressure at a level that will assure adequate blood flow to all the peripheral tissues

How well heart does this task = cardiac performance

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2
Q

Left ventricular pulse pressure

A

Get through left ventricular catheterization

Mainly done through radial artery

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3
Q

Pressure/volume loop

A

Plots pressure as function of volume

Time flows in counter clockwise direction

Xaxis volume
Yaxis pressure

Use a tool to compute work done by ventricular
Area of loop = work done by ventricle

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4
Q

LVPP

A

Diff btw systolic and diastolic pressure

LVPP = systolic p - diastolic p

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5
Q

Factors that influence CO

A

Preload
Afterload
Contractility

ANS (impacts HR and contractility)

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6
Q

Preload

A

Tension in ventricular wall at end of diastole (proportional to EDV)

Tension usually not determined
Therefore measure
Ventricular EDV or
Ventricular ED pressure

Determines resting fiber length

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7
Q

Importance of preload

A

Regulation of CO is based on the observation that strength of contraction of an isolated cardiac muscle fiber is a function of muscle fiber length ( length tension relationship)

Frank-starling law of the heart

As increase EDV heart is intrinsically able to eject more blood

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8
Q

Frank-starling

A

Relationship manifested in the length tension relationship

Thought to be due to the increased number of XBs formed

As EDV increases, ventricle contracts w more force and a greater SV results

Place on curve means able to accommodate variation in volumes

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9
Q

Frank-starling also ensures

A

The outputs of the right and left ventricle are matched

Has to match

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10
Q

Increasing volume load (preload)

A

Also increase EDV

Increases stoke volume SV
ESV doesn’t change

There’s a peak pressure that ventricle can generate

Area within loop is LVSW
Increases ventricular work

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11
Q

Factors that determine preload

A

Ventricular filling time - dependent on HR (increase HR, EDV (&SV) May decrease

Ventricular compliance - (change V/change P) low compliance can impede filling

Filling pressure- w neg intrathoracic P, increase venous return to right heart

Contribution of atrial systole to filling- important when filling time is reduced

Pericardial constraint- increases fluid around heart can reduce compliance and filling

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12
Q

Ventricular filling time and preload

A

Time available for passive filling

In absence of sympathetic stimulation
(Langendorff heart prep)
Increase HR to 150 bpm lowers time for reduced filling
CO usually not affected since decreases SV compensated for by increased HR
CO adversely affect at HR >150 -180 bpm

With sympathetic stimulation (in vivo)
SV preserved due to increased contractility
CO can increase dramatically

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13
Q

Ventricular compliance and preload

A

Ability of ventricle to distend under pressure

Highly compliant chamber will undergo a large change in volume with relatively small change in pressure

Low compliance ventricles develop higher pressures during diastole which retard filling

Compliance is reduced in hypertrophy and ischemia

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14
Q

Ventricular filling pressure and preload

A

Pressure gradient between inside and outside of ventricle

Intrathoracic pressure and central venous pressure (CVP) affect right ventricular pressure and SV

Decreasing intrathoracic pressure (I.e. inspiration) or increasing CVP will increase RV preload and therefore SV

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15
Q

Atrial systole and preload

A

Atrial systole and contractility have small effect on EDV
only responsible for 10-25% of EDV
atrial kick

Atrial systole can be very important in cases where diastole filling times are limited
When rapid filling times are reduced (high HR)
Sympathetic stimulation can increase atrial contractility

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16
Q

Pericardial constraint and preload

A

Role of pericardium w respect to EDV
protects against left ventricular volume overload
Maintains alignment w major vessels
( has minimal fluid)

If pericardium becomes filled with excess fluid:
Fluid will exert a hydrostatic pressure on the external surface of heart that effectively reduces ventricular compliance
Lowered compliance reduces EDV and SV
EX: cardiac tamponade

17
Q

Determinant of cardiac performance: afterload

A

Resistance against which ventricle contracts (resistance heart has to overcome to eject blood into aorta)

For left ventricle, major components: 
Arterial pressure 
Peripheral vascular resistance (PVR) 
Arterial wall compliance 
Mass of the column of blood in aorta 
Viscosity of blood

Estimated by mean arterial pressure = DP + 1/3PP

18
Q

Inverse relationship btw afterload and

A

Ventricular muscle shortening (SV)

Maximum velocity of ejection

19
Q

Increased afterload w constant EDV

A

Aortic valve opens later and closes sooner

Increases ESV

reduces SV

20
Q

Clinically

Afterload is increased by

A 
Aortic stenosis 
Elevated arterial pressure 
Increase PVR 
increase blood viscosity
Decrease arterial compliance
21
Q

Physiological compensation: increased afterload

A

Increased ESV, ventricle still fills normally so EDV increases

Restores normal SV

Increased area in the loop=increased ventricular stroke work

22
Q

Determinants of cardiac performance

Contractility

A

Ability of heart to do work at any given fiber length

Distinct from changes in EDV/preload and afterload/arterial pressure

Factors that affect myocardial contractility:
ANS activity (primarily SNS)
Circulating hormones (I.e. epinephrine)
Catechilamines increase Ca influx and availability (more x bridges = more force generated)
23
Q

Fiber length proportional to

A

EDV

compare curves holding EDV constant

SNS stimulation:
Increase SV at any given EDV
Increases ejection fraction
Positive inotropic effect

24
Q

SNS stimulation also increase

A

Rate of rise (+dP/DT)

Also rate of rise (-dP/DT) enhances 
  Shortens systole (filling times maintained)
25
Q

Effects of increasing contractility (I.e. SNS)

A

At any give EDV, EDP, and afterload ventricle:
Ejects more blood (increases SV) due to more rapid/forceful emptying

Increased contractility will increase ejection fraction and decrease ESV

26
Q

ESV dependent upon

A

Afterload and contractility

Contractility increases(velocity of shortening increases:
Increases ejection velocity, SV
Decrease ESV

Conversely decrease contractility:
Increase ESV
Decrease SV

27
Q

Assessment contractility

A

Can’t measure wall tension directly

Can measure isovolumic indices (get rate of ventricular P changes during isovolumic contraction (+dP/dt) with catheterization

Can measure ejection indices:
Ejection fraction through echocardiography 
Ratio of SV to EDV 
  Normal 50-75%
  Abnormal <40%
28
Q

HR influences cardiac performance in 2 ways

A

Treppe

Relationship btw HR and CO redux

29
Q

Treppe

A

Aka Bowditch staircase effect

Increasing HR causes Ca accumulation, increases contractility

More Ca enters per unit time at high HR and some is stored in SR

available for release on subsequent beats

Helps maintain CO at very fast HRs

Small but measurable effect

30
Q

Relationship btw work load and HR

A

HR increases linearly w exercise intensity

Max HR a function of age , not training

31
Q

Relationship btw work load and SV

A

SV is linear at low intensities but plateaus

Plateau likely due to reduced ventricular filling time

32
Q

Cardiac metabolism

A

Resting metabolic rate
25% to basal metabolism, rest for contraction
MR increases during heavy exercise
Cardiac muscles have many mitochondria & capillaries
Left ventricle does 6-7x work of right

Substrates:
35-40% energy requirement from carb ox under basal, fasted conditions
Balance of energy primarily from fatty acid ox (fasted)
Highly aerobic

33
Q

During exercise

A

Efficiency improves

Volume work increases; energetically less costly than pressure work

34
Q

Volume work

A

Moving blood / preload

35
Q

Pressure work

A

Working against afterload

Physio Exam 3 (9 decks)

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